Orthostatic (postural) hypotension: causes, symptoms, diagnosis, treatment

Orthostatic (postural) hypotension is a sudden drop in blood pressure (usually more than 20/10 mm Hg) when the patient assumes a vertical position. Fainting, loss of consciousness, confusion, dizziness, and visual impairment may occur within a few seconds or over a longer period. Some patients experience serial syncope. Physical exertion or heavy meals may trigger such conditions. Most other manifestations are related to the underlying cause. Orthostatic hypotension is a manifestation of abnormal regulation of blood pressure caused by various reasons rather than a single disease.

Orthostatic hypotension occurs in 20% of elderly people. It may be more common in people with comorbidities, primarily hypertension, and in patients who have been on bed rest for a long time. Many falls occur due to unrecognized orthostatic hypotension. The manifestations of hypotension are aggravated immediately after eating and stimulation of the vagus nerve (e.g., after urination, defecation).

Postural orthostatic tachycardia syndrome (POTS), or so-called spontaneous postural tachycardia, or chronic or idiopathic orthostatic reaction, is a syndrome of pronounced predisposition to orthostatic reactions at a young age. Standing up is accompanied by the appearance of tachycardia and various other symptoms (such as weakness, dizziness, inability to perform physical activity, clouding of consciousness), while blood pressure decreases by a very small amount or does not change. The cause of the syndrome is unknown.

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Causes of Orthostatic Hypotension

Mechanisms for maintaining homeostasis may not be able to restore arterial pressure if the afferent, central or efferent link of autonomic reflexes is impaired. This may occur when taking certain medications, if myocardial contractility or vascular resistance are depressed, or in hypovolemia and dyshormonal conditions.

The most common cause in older people is a combination of decreased baroreceptor sensitivity and arterial lability. Decreased baroreceptor sensitivity leads to a decrease in the severity of cardiac responses when taking a vertical position. Paradoxically, arterial hypertension can be one of the causes of decreased baroreceptor sensitivity, increasing the tendency to orthostatic hypotension. Postprandial hypotension is also common. It can be caused by the synthesis of large amounts of insulin when consuming carbohydrate-containing foods, as well as by blood flow to the gastrointestinal tract. This condition is aggravated by alcohol intake.

Causes of Orthostatic Hypotension

Neurological (including autonomic dysfunction)

Central	Multifocal system atrophy (formerly Schaich-Dreger syndrome). Parkinson's disease. Strokes (various)
Spinal cord	Tabes dorsalis. Transverse myelitis. Tumors
Peripheral	Amyloidosis. Diabetic, alcoholic or nutritional neuropathy. Familial autonomic dysfunction (Riley-Day syndrome). Guillain-Barre syndrome. Paraneoplastic syndromes. Severe autonomic failure (previously called idiopathic orthostatic hypotension). Surgical sympathectomy

Cardiology

Hypovolemia	Adrenal insufficiency. Dehydration. Blood loss
Vasomotor tone disorder	Long-term fatigue. Hypokalemia
Cardiac output disorders	Aortic stenosis. Constrictive pericarditis. Heart failure. THEM. Tachy and bradyarrhythmias
Other	Hyperaldosteronism*. Peripheral venous insufficiency. Pheochromocytoma*

Medicines

Vasodilators	Calcium channel blockers. Nitrates
Affecting sympathetic regulation	A-Blockers (prazosin). Antihypertensive agents (clonidine, methyldopa, reserpine, sometimes P-blockers). Antipsychotics (mainly phenothiazines). Monoamine oxidase inhibitors (MAOIs). Tricyclic or tetracyclic antidepressants
Other	Alcohol. Barbiturates. Levodopa (rarely in patients with Parkinson's disease). Loop diuretics (eg, furosemide). Quinidine. Vincristine (due to neurotoxicity)

*Can cause arterial hypotension in a horizontal position. Symptoms are more pronounced at the beginning of treatment.

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Pathophysiology of orthostatic hypotension

Normally, gravitational stress from standing up quickly causes a certain amount of blood (0.5 to 1 liter) to move into the veins of the lower extremities and trunk. The subsequent transient decrease in venous return reduces cardiac output and, consequently, blood pressure. The first manifestations may be signs of decreased blood supply to the brain. At the same time, a decrease in blood pressure does not always lead to cerebral hypoperfusion.

The baroreceptors of the aortic arch and carotid zone respond to arterial hypotension by activating autonomic reflexes aimed at restoring arterial pressure. The sympathetic nervous system increases the heart rate and myocardial contractility. Then the tone of the accumulative veins increases. At the same time, the parasympathetic reactions are inhibited to increase the heart rate. If the patient continues to stand, the renin-angiotensin-aldosterone system is activated and antidiuretic hormone (ADH) is secreted, resulting in the retention of sodium and water ions and an increase in the volume of circulating blood.

Diagnosis of orthostatic hypotension

Orthostatic hypotension is diagnosed when a decrease in measured arterial pressure and the appearance of clinical signs of arterial hypotension upon standing up and the disappearance of these symptoms upon assuming a horizontal position are noted. The causes must be identified.

Anamnesis

The patient is questioned to identify known precipitating factors (e.g. medication, prolonged bed rest, fluid loss) and symptoms of autonomic failure [such as visual changes in the form of mydriasis and accommodation disorders, urinary incontinence, nausea, poor heat tolerance (excessive sweating), impotence]. Other neurological symptoms, cardiovascular disorders, and mental dysfunction should also be noted.

Physical examination. Blood pressure and heart rate are measured 5 minutes after the patient assumes a horizontal position, as well as 1 and 3 minutes after standing up. If the patient cannot stand, he or she is examined in a sitting position. Arterial hypotension without a compensatory increase in heart rate (< 10 per minute) indicates impaired reflexes, a marked increase (> 100 per minute) indicates hypovolemia or, if symptoms develop without hypotension, POTS. Other findings may be signs of dysfunction of the nervous system, including parkinsonism.

Additional research methods. Routine research in this case includes ECG, glucose concentration determination and electrolyte composition of blood plasma. At the same time, these and other studies are usually uninformative compared to specific clinical symptoms.

It is necessary to clarify the state of the autonomic nervous system. When it functions normally, an increase in heart rate is noted during inhalation. To clarify the state, the patient's cardiac activity is monitored during slow and deep breathing (about 5 min - inhalation, 7 sec - exhalation) for 1 min. The longest RR interval during exhalation is normally 1.15 times longer than the minimum interval during inhalation. Shortening of the interval indicates an autonomic disorder. Similar differences in duration should be present when comparing the rest period and the 10-15-second Valsalva maneuver. Patients with an abnormal RR interval or other signs of autonomic dysfunction require further examination to exclude diabetes mellitus, Parkinson's disease, possibly multiple sclerosis and severe autonomic insufficiency. The latter may require a study of the amount of norepinephrine or vasopressin in the blood plasma of patients in horizontal and vertical positions.

The inclined surface test (inclined table) is less variable than the measurement of blood pressure in the vertical and horizontal position, and allows to exclude the influence of leg muscle contractions on venous return. The patient can be in the vertical position for up to 30-45 minutes, during which time blood pressure is measured. The test can be performed if there is a suspicion of a disorder of vegetative regulation. To exclude drug etiology, the amount of drugs capable of causing orthostatic hypotension should be reduced or completely discontinued.

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Prevention and treatment of orthostatic hypotension

Patients who must remain in bed for long periods should sit up in bed daily and exercise whenever possible. Patients should rise slowly from a sitting or lateral position, drink adequate fluids, limit or abstain from alcohol, and exercise whenever possible. Regular moderate-intensity exercise increases peripheral vascular tone and reduces blood pooling. Elderly patients should avoid prolonged standing. Sleeping with the head of the bed elevated may reduce symptoms by increasing sodium retention and reducing nocturia.

Postprandial hypotension can often be prevented by reducing the total amount of food consumed and its carbohydrate content, minimizing alcohol intake, and avoiding standing up abruptly after eating.

Tight high bandaging of the legs with an elastic bandage can increase venous return, cardiac output and blood pressure after standing up. In severe cases, an inflatable suit similar to antigravity suits for pilots can be used to create the necessary compression of the legs and abdomen, especially in cases of severe resistance to treatment.

Increasing the sodium content, resulting in an increase in circulating blood volume, may help to reduce symptoms. In the absence of heart failure and arterial hypertension, the sodium ion content can be increased from 5 to 10 g by simply increasing its intake with food (more salt in food or taking sodium chloride tablets). This prescription increases the risk of developing heart failure, especially in elderly patients and patients with impaired cardiac function; the occurrence of edema due to this method of treatment without the development of heart failure is not considered a contraindication to continuing treatment.

Fludrocortisone, a mineralocorticoid that causes sodium retention, increases plasma sodium levels, and often reduces hypotension, is effective only if sodium intake is adequate. The dose is 0.1 mg at night, increased weekly to 1 mg or until peripheral edema occurs. This drug can also enhance the peripheral vasoconstrictor effect of sympathetic stimulation. Lying hypertension, heart failure, and hypokalemia may occur. Potassium supplementation may be necessary.

Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin at a dose of 25-50 mg/day, can inhibit prostaglandin-induced vasodilation, increasing peripheral vascular resistance. It should be remembered that NSAIDs can cause damage to the gastrointestinal tract and cause vasopressor reactions (there are reports of equivalence of indomethacin and sympathomimetics).

Propranolol and other beta-blockers may enhance the beneficial effects of sodium and mineralocorticoid therapy. Propranolol's blockade of beta-adrenergic receptors results in uncontrolled a-adrenergic vasoconstriction, which prevents orthostatic vasodilation in some patients.